Thromboplastin and

Most laboratories report results for the INR along with the patient s PT and the control value. The INR was devised as a way to standardize PT values and represents a way to correct the routine PT results from different laboratories using various sources of thromboplastin and methods of preparation for the test. The INR is determined by a mathematical equation comparing the patient s PT with the standardized PT value. Some institutions may use only PT, others PT/INR, and some may use INR. The INR is maintained between 2 and 3. 

Thromboplastin A substance that triggers the coagulation cascade. Tissue factor is a naturally-occurring thromboplastin and is used in the prothrombin time test. 

Vitamin K activity is associated with several quinones, including phylloquinone (vitamin Kj), menadione (vitamin K3), and a variety of menaquinones (vitamin K2). These quinones promote the synthesis of proteins that are involved in the coagulation of blood. These proteins include prothrombin, factor VII (proconvertin), factor IX (plasma thromboplastin), and factor X (Stuart factor). A detailed discussion of blood coagulation is found in Chapter 22. The vitamin K quinones are obtained from three major sources. Vitamin K is present in vari-... 

R — time corresponding to invisible phases of clotting process, thromboplastin and thrombin formation, cm 2.0 19.0... 

Uses. Warfarin is the oral anticoagulant of choice, for it is reliably effective and has the lowest incidence of adverse effects. Monitoring of therapy is by the prothrombin time. Usually the test is carried out with a standardised thromboplastin and the result is expressed as the International Normalised Ratio (INR), which is the ratio of the prothrombin time in the patient to that in a normal (non-anticoagulated) person—taking account of the sensitivity of the... 

Disorders of fibrinogen also occur in the liver. For example, dysfibrinogenemia may be seen in both acute and chronic liver disease and leads to prolongation of the partial thromboplastin time, Disseminated intravascular coagulation occurs with acute hepatic necrosis, presumably as a result of the release of tissue thromboplastin and defective clearance of inhibitors such as antithrombin and protein C. Thrombocytopenia may contribute to ineffective intravascular coagulation. Although commonly attributed to splenic sequestration (hypersplenism), there is evidence of antibody-mediated platelet destruction, as occurs in... 

Functional evaluation of the extrinsic and final common pathways. Time for clot formation is determined after addition of thromboplastin and Ca + to a plasma sample. 

When blood is lost or clotting is initiated in some other way, a complex cascade of biochemical reactions is set in motion, which ends in the formation of a network or clot of insoluble protein threads enmeshing the blood cells. These threads are produced by the polymerisation of the molecules of fibrinogen (a soluble protein present in the plasma) into threads of insoluble fibrin. The penultimate step in the chain of reactions requires the presence of an enzyme, thrombin, which is produced from its precursor prothrombin, already present in the plasma. This is initiated by factor lit (tissue thromboplastin), and subsequently involves various factors including activated factor Vn, DC, X, XI and XII, and is inhibited by antithrombin in. Platelets are also involved in the coagulation process. Fibrinolysis is the mechanism of dissolution of fibrin clots, which can be promoted with thrombolytics. For further information on platelet aggregation and clot dissolution, see Antiplatelet drugs and thrombolytics , (p.697). 

Expression of tissue thromboplastin and urokinase-type plasminogen activator (EC 3.4.21.73) receptor were stimulated in monocyte-like U-937 cells treated with 5 ng 12-0-tetradecanoylphorbol-13-acetate per ml (Haase et al. 1993). 

According to Seegers [4], the conversion of prothrombin to thrombin can be catalyzed by a two-enzyme system, thromboplastin and thrombin itself. The compounds participating in this reaction [5-8] are somewhat better known than those involved in thromboplastin formation (prothrombin activator). 

During blood coagulation, prothrombin is activated to yield thrombin. Tissue thromboplastin and calcium are required for the activation. The exact mechanism of activation is not known, and little information is available on the product of the activation—thrombin. 

A protein which converts fibrinogen to fibrin, the fibrous material of the blood clot. Thrombin itself is formed from prothrombin by the action of thromboplastin and calcium. 

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